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 Previous Article
Journal of Neuroscience, Vol 12, 2000-2006, Copyright © 1992 by Society for Neuroscience
5-hydroxytryptamine1B receptors block the GABAB synaptic potential in rat dopamine neurons
SW Johnson, NB Mercuri and RA North
Vollum Institute, Oregon Health Sciences University, Portland 97201.
Intracellular recordings were made from presumed dopamine-containing
neurons in slices cut from the midbrain of the rat. Focal electrical
stimulation produced a hyperpolarizing synaptic potential that was reduced
by 75-95% by the GABAB-receptor antagonist 2-hydroxysaclofen (300 microM).
5-HT (3-100 microM) reduced the amplitude of the GABAB synaptic potential
by 20-74%, with a 50% reduction at 10 microM, but did not reduce the
amplitude of synaptic potentials mediated by GABAA receptors. 5-HT acted
presynaptically because hyperpolarizations produced by exogenously
administered GABA (1 mM) in picrotoxin (100 microM) were not affected by
5-HT (30 microM). (+/-)-Cyanopindolol (100 nM), a 5-HT1B antagonist,
blocked the effect of 5-HT (10 microM); spiperone (1 microM), which is an
antagonist at 5-HT1A and 5-HT2 receptors, had no effect. The amplitude of
the GABAB synaptic potential was reduced by the 5-HT1B receptor agonists
1-[3-(trifluoromethyl)- phenyl]-piperazine (300 nM) and
7-trifluoromethyl-4-(4-methyl-1- piperazinyl)-pyrrolo[1,2-a]quinoxaline (1
microM), but not by the 5- HT1A agonist
N,N-dipropyl-5-carboxamidotryptamine (1 microM) or the 5- HT2 agonist
(+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-amino-propane (10 microM). We
conclude that 5-HT activates presynaptic 5-HT1B receptors that inhibit the
release of GABA onto GABAB but not GABAA receptors.
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